ABSTRACT
Bullying victimisation is an increasing global health problem among adolescents and is associated with short- and long-term adverse mental health outcomes. Investigating whether associations with mental health vary across national contexts and why, can provide insights into mechanisms underlying those associations and inform policy. We used data from 479,685 adolescents participating in the 2018 Program for International Student Assessment (PISA) cross-sectional survey and examined whether the associations between bullying victimisation, psychological distress and life satisfaction vary across 63 countries. We further tested the modifying role of country-level factors - bullying prevalence, income inequality and national wealth, by implementing multilevel cross-country analyses. We found significant associations between bullying victimisation, increased psychological distress (ß = 0.181; 95%CI: 0.178, 0.184) and decreased life satisfaction (ß = -0.158; 95%CI: -0.162, -0.155). Associations between bullying victimisation, psychological distress and life satisfaction among adolescents were consistent across countries in terms of direction but effect sizes varied substantially. The effects ranged from ß = 0.08 in the Philippines to ß = 0.40 in South Korea for psychological distress and from ß = -0.05 in the Philippines to ß = -0.36 in the United Kingdom for life satisfaction. In addition, consistent with the "healthy context paradox" effect, associations between bullying and mental health were larger in countries where the prevalence of bullying was lower, as well as in higher-income countries. Interventions aiming to reduce bullying victimisation should aim to provide additional targeted support for those who still experience bullying after the intervention.
ABSTRACT
BACKGROUND: Genetic influences are ubiquitous as virtually all phenotypes and most exposures typically classified as environmental have been found to be heritable. A polygenic score summarises the associations between millions of genetic variants and an outcome in a single value for each individual. Ever lowering costs have enabled the genotyping of many samples relevant to child psychology and psychiatry research, including cohort studies, leading to the proliferation of polygenic score studies. It is tempting to assume that associations detected between polygenic scores and phenotypes in those studies only reflect genetic effects. However, such associations can reflect many pathways (e.g. via environmental mediation) and biases. METHODS: Here, we provide a comprehensive overview of the many reasons why associations between polygenic scores, environmental exposures, and phenotypes exist. We include formal representations of common analyses in polygenic score studies using structural equation modelling. We derive biases, provide illustrative empirical examples and, when possible, mention steps that can be taken to alleviate those biases. RESULTS: Structural equation models and derivations show the many complexities arising from jointly modelling polygenic scores with environmental exposures and phenotypes. Counter-intuitive examples include that: (a) associations between polygenic scores and phenotypes may exist even in the absence of direct genetic effects; (b) associations between child polygenic scores and environmental exposures can exist in the absence of evocative/active gene-environment correlations; and (c) adjusting an exposure-outcome association for a polygenic score can increase rather than decrease bias. CONCLUSIONS: Strikingly, using polygenic scores may, in some cases, lead to more bias than not using them. Appropriately conducting and interpreting polygenic score studies thus requires researchers in child psychology and psychiatry and beyond to be versed in both epidemiological and genetic methods or build on interdisciplinary collaborations.
